Turkish Journal of Medical Sciences
Turk J Med Sci
(2014) 44: 178-185
Research Article
Cystatin C as biomarker of contrast-induced nephropathy in pediatric cardiac angiography
Osman ÖZDEMİR *, Ayşe Deniz OĞUZ , Abdülkadir EREN ,
Cihat ŞANLI , Hüsnü Oğuz SÖYLEMEZOĞLU , Ayşe Banu ÇAYCI
Department of Pediatric Cardiology, Keçiören Training and Research Hospital, Ankara, Turkey
Department of Pediatric Cardiology, Faculty of Medicine, Gazi University, Ankara, Turkey
Department of Pediatrics, Faculty of Medicine, Gazi University, Ankara, Turkey
Department of Pediatrics, Faculty of Medicine, Kırıkkale University, Kırıkkale, Turkey
Department of Pediatric Nephrology, Faculty of Medicine, Gazi University, Ankara, Turkey
Department of Biochemistry, Faculty of Medicine, Gazi University, Ankara, Turkey
Received: 09.10.2012
Accepted: 21.06.2013
Published Online: 15.01.2014
Printed: 14.02.2014
Background/aim: The purpose of this study is to find the frequency of contrast-induced nephropathy (CIN) and to show the risk factors
in the development of CIN and the diagnostic utility of serum cystatin C (CysC) and serum and urine neutrophil gelatinase-associated
lipocalin (NGAL) during childhood following cardiac angiography.
Materials and methods: In this prospective study, we studied 46 children with congenital heart disease. The levels of serum creatinine,
serum CysC, and serum NGAL were measured at 4, 24, and 48 h, while levels of urine NGAL and urine creatinine were measured at 4
to 8 and 48 h following cardiac angiography.
Results: According to serum creatinine levels, with a cutoff value of 4.1 mL/kg for development of CIN, sensitivity, specificity, area
under the receiver-operating characteristic curve, and positive likelihood ratio were calculated as 69%, 70%, 0.67, and 2.29, respectively.
The levels of serum CysC and serum creatinine significantly increased at 4, 24, and 48 h after the application of the contrast agent.
Conclusion: The results of this study show that according to the definition of CIN, the incidence of CIN is significantly increased in
pediatric patients with congenital heart disease. Moreover, the results support that serum CysC levels may allow the detection of CIN
after cardiac angiography, like serum creatinine in present study.
Key words: Cardiac angiography, contrast media, creatinine, cystatin C, lipocalin, nephropathy
1. Introduction
The administration of radiographic contrast agents
remains an important cause of hospital-acquired acute
renal failure, which contributes to morbidity and mortality
during hospitalization, prolongs hospital stay, and
increases the incidence of chronic end-stage renal disease
and costs of health care (1–5). In pediatric studies, the
acute renal damage induced by nephrotoxins is estimated
to have been 17%, half of which was reported to result
from cardiac angiography (6). Twelve percent of acute
renal failures were shown to be induced by the use of
contrast media (3). Therefore, in all intervention contrast
media used, risks for nephropathy should be evaluated and
necessary precautions should be taken for the patients.
In recent studies, cystatin C (CysC) and neutrophil
gelatinase-associated lipocalin (NGAL) were defined as
determining the renal damage risk (7,8). It has been shown
*Correspondence: [email protected]
that, in diagnosing contrast-induced nephropathy (CIN),
the level of serum CysC in the first 24–48 h and the serum
and urine NGAL levels in the first 4 h have seen to have
increased (9–12).
In this study, we aimed to evaluate the incidence
and risk factors for CIN in children undergoing cardiac
angiography, and the role of serum CysC and serum and
urine NGAL levels in early diagnosis of CIN.
2. Materials and methods
2.1. Study population
This study was conducted within a period of 18 months
on 13 healthy children whose physical examination was
found to be within normal limits and on 46 subsequent
patients with congenital heart disease, whose diagnostic
cardiac angiographies were carried out in the Pediatric
Cardiology Department of the Medical Faculty of Gazi
ÖZDEMİR et al. / Turk J Med Sci
University. Prior to this study, which was prepared in
compliance with the Declaration of Helsinki and supported
by the Scientific Research Projects Unit at Gazi University
with the permission of the local ethics council, informed
consent was obtained from the parents of the children.
The age, sex, body weight, body height, body surface
area, medication history, cyanosis, systolic and diastolic
blood pressure, and echocardiographic left ventricular
ejection fraction of the patients were recorded 24 h prior
to the angiography procedure. Blood samples for complete
blood count, urea, creatinine, serum CysC level, and serum
NGAL level and urine samples for urine specific gravity,
urine creatinine level, and urine NGAL level were taken.
Glomerular filtration rate was calculated. Oral feeding
was stopped while intravenous hydration (1500–2000
mL m–2 day–1) was started 4–8 h prior to the procedure.
Intravenous hydration with isotonic saline solution was
continued for 24 h after the procedure.
Standing height (cm) was measured to the nearest
0.1 cm using a Harpenden fixed stadiometer. Body weight
(kg) was observed on a SECA balance scale to the nearest
0.1 kg, with subjects dressed in underwear. The body
surface area was calculated using the DuBois formula (13).
Blood pressure was measured with a standard clinical
sphygmomanometer (ERKA, Germany) from the right
arm after a 5-min rest in the supine position, using a
stethoscope placed over the brachial artery pulse, proximal
and medial to the cubital fossa, and below the bottom edge
of the cuff (i.e. 2 cm above the cubital fossa). The cuff
used was appropriate for the size of the child’s upper right
arm (14). Transthoracic echocardiography was examined
with ViVid 7 Pro (General Electric Medical Systems,
USA) and 5- and 7-MHz transducers, according to the
recommendations of Task Force of the Pediatric Council
of the American Society of Echocardiography (15).
2.2. Study design
Blood samples were drawn from the antecubital vein in all
subjects. For the serum urea and creatinine levels, Abbott
ARCHITECT c16000 and assay kits were used (Abbott,
USA). The glomerular filtration rate (with respect to
the reference interval of 60–169 mL min–1 1.73 m–2) was
calculated using the Schwartz formula (16). The blood
count, from blood taken into tubes with special lids
including potassium ethylene diamine tetraacetic acid,
was conducted using the CELL-DYN Sapphire and CELLDYN 3700 models of Abbott. The urine specific gravity
(with respect to the reference interval of 1002–1030) was
evaluated using the Roche Combur10 Test and Miditron M.
Serum NGAL levels (with respect to the reference interval
of 19.99–148.94 ng/mL) and urine NGAL levels were
examined with a fully automated ALISEI ELISA device
(SEAC Diagnostics, Italy) using the commercial ELISA
human lipocalin-2/NGAL kit (Biovendor Research and
Diagnostic Products, Czech Republic). Urine creatinine
measurements were conducted using original Olympus
kits in an Olympus AU400 immunoanalyzer (Japan).
Serum CysC levels (with respect to the reference interval
of 0.53–0.95 mg/L) were determined using a nephelometer
produced by Siemens (BN II System, Germany) with
Siemens N Latex Cystatin C Kits.
Cardiac angiography procedures were initiated
with sedation and local anesthesia with strict aseptic
preparation of the skin. The sheaths were percutaneously
inserted into the femoral vein and artery. Pressure records
and blood samples were taken from each location of the
heart and vessels via appropriate cardiac catheters. After
administering contrast media injections, angiograms were
taken, nephrograms having been recorded. Iopromide
(769 mg/mL Ultravist-370, IV flacon, Schering German
Pharmaceutical Company) was intravenously used as
a contrast medium with nonionic low osmolarity. The
amount of the contrast medium during the procedure,
fluoroscopy time, and oxygen saturations of the patients
were all recorded. Blood samples were taken at the end
of 4, 24, and 48 h for serum creatinine, serum CysC, and
serum NGAL levels. Urine samples were taken at 4–8 h
and at the end of 48 h for urine NGAL and urine creatinine
levels. Serum creatinine, serum CysC, and serum and
urine NGAL levels were also taken into account in the
healthy children in the control group as well.
For the diagnosis of CIN, ≥25% relative increase or
an absolute increase of ≥0.5 mg/dL in serum creatinine
from baseline value at 48 to 72 h after exposure to contrast
media when alternative explanations for renal impairment
or kidney failure had been excluded was used (2–4).
2.3. Statistical analyses
SPSS, 16.01 for Windows (SPSS Inc., USA) was used for
statistical analyses. All data were reported as mean ±
standard deviation. In comparing the patient and control
group data, the Mann–Whitney U test, a nonparametric
test, was used; for the data for the 2 dependent groups, the
Wilcoxon signed-rank test (Kruskal–Wallis analysis was
used; and for the data having more than 2 dependent group
parameters, the Friedman repeated measures analysis of
variance (ANOVA) test was used for evaluations. Having
completed the Friedman ANOVA, the Wilcoxon signedrank test with Bonferroni correction was implemented in
order to show from which group the statistical discrepancy
had stemmed. When the general significance level was
regarded as <0.05, the P-value, considered statistically
significant in correlations with more than 2 variables, was
acquired by dividing the value into the number of the groups
compared (P < 0.05/number of the groups compared). In
comparing the ratios of the groups, the chi-square test was
implemented. For multivariate analysis of CIN risk factors,
backward stepwise logistic regression analysis was used. To
ÖZDEMİR et al. / Turk J Med Sci
measure the sensitivity and specificity for contrast medium
volume for development of CIN, receiver-operating
characteristic (ROC) curves were generated and the area
under the curve (AUC) calculated. An AUC of 0.5 is not
accepted as a risk factor, whereas a value of 1.0 signifies a
perfect cutoff volume of contrast medium. P values of less
than 0.05 were considered statistically significant.
3. Results
Forty-six patients (18 males and 28 females) using contrast
media whose median age was 3 years (2 months to 16
years) and 13 healthy children (6 males and 7 females)
whose median age was 6 years (9 months to 13 years) were
studied. In the patients, the medians of weight, height, and
body surface area were found 14.5 kg, 95 cm, and 0.61 m2,
respectively. In the controls, these were 18 kg, 110 cm, and
0.70 m2, respectively.
The clinic and laboratory data are summarized in
Table 1. There was no significant difference (P > 0.05) in
blood pressures; urine specific gravity; serum creatinine;
glomerular filtration rate; serum CysC, serum NGAL, and
urine NGAL levels; or urine NGAL/urine creatinine ratio
between the patients and healthy children. Furthermore,
anaphylactic reaction, acute renal failure, morbidity, and
mortality were not observed in the patients.
Sixteen subjects who received cardiac angiography with
contrast media and who developed CIN (≥25% increase in
serum creatinine from baseline value) and 30 children with
no CIN were compared in terms of risk factors (Table 2).
No significant difference was found between the groups in
this comparison (P > 0.05). The risk factors for CIN were
then evaluated with backward stepwise logistic regression
analysis (Table 3), but these factors were not independent
risk factors. The diagnoses of the patients are shown in
Table 4.
A cutoff volume of contrast media was found as 4.1
mL/kg in the patients with CIN. The sensitivity, specificity,
negative predictivity, and positive predictivity of the
cutoff volume were calculated as 69%, 70%, 51%, and
50%, respectively. The AUC of ROC curves and positive
likelihood ratio were found as 0.67 (range: 0.51 to 0.84)
and 2.29 for the cutoff volume of contrast media.
The nephrotoxicity findings in the patients with and
without CIN are compared in Table 5. The serum creatinine
and CysC levels at all measurement times were within
normal ranges. However, serum creatinine and serum
CysC levels in the subjects with CIN after the procedure at
4, 24, and 48 h were statistically found to be significantly
high in comparison to the values prior to angiography (P <
0.05), whereas no significant difference was found in other
comparisons (P > 0.05).
4. Discussion
CIN is typically defined as an increase in serum creatinine
by either ≥0.5 mg/dL or by ≥25% from baseline within the
first 2–3 days after contrast administration (2,4). In line
with this definition, in 16 of the subjects who underwent
cardiac angiography (34.7%) in our study, the basal serum
creatinine level was found to have increased by 25% or
more. In 3 of these patients (6.5%), an increase of 50% or
more in creatinine levels were observed. However, serum
creatinine levels did not increase by higher than 0.5 mg/dL
from baseline levels in the patients. After the angiography,
we found significantly high levels of serum creatinine and
serum CysC at 4, 24, and 48 h compared to the values prior
to the procedure in the patients diagnosed with CIN.
Despite the fact that there are no comprehensive studies
done on CIN in large pediatric patient groups, it is known
that CIN is the third most widespread reason for acute
renal cases developing in hospitals, with 12% of contrast
Table 1. Comparisons of basal clinical and laboratory findings between the groups.
Patients (n = 46)
Controls (n = 13)
Systolic blood pressure, mmHg
92.5 (60–140)
90 (70–110)
Diastolic blood pressure, mmHg
60 (40–80)
50 (40–70)
Urine specific gravity
1010 (1005–1035)
1010 (1005–1020)
Serum creatinine, mg/dL
0.45 (0.31–0.79)
0.48 (0.36–0.72)
GFR, mL min–1 1.73 m–2
120 ± 35.9
113 ± 25.2
Serum cystatin C, mg/L
0.56 (0.3–1.1)
0.55 (0.4–0.8)
Serum NGAL, ng/mL
32.0 (1.9–226)
35.1 (18.3–90.3)
Urine NGAL, ng/mL
2.5 (0.6–67.1)
1.8 (0.6–16.4)
Urine NGAL/urine creatinine, ng/mg
3.9 (1.2–47.6)
3.2 (0.8–49.8)
: Mann–Whitney U test; P < 0.05.
GFR: glomerular filtration rate; NGAL: neutrophil gelatinase-associated lipocalin.
ÖZDEMİR et al. / Turk J Med Sci
Table 2. Comparisons of risk factors of contrast-induced nephropathy in the patients.
Risk factors
No CIN (n = 30)
CIN (n = 16)
Number of patients with drug use
4 (13.3%)
2 (12.5%)
Number of patients with cyanosis
4 (13.3%)
5 (31.3%)
Number of patients with anemia
7 (23.3%)
7 (43.8%)
Mean ± SD of hemoglobin, g/dL
12.3 ± 1.2
12.2 ± 1.8
Mean ± SD of hematocrit, %
36.7 ± 3.4
36.6 ± 4.3
Median of ejection fraction, %
71.5 (25–81)
72 (62–85)
Median of contrast media volume, mL
57.5 (20–165)
58 (10–153)
Mean ± SD of contrast media volume, mL/kg
3.7 ± 2.0
5.0 ± 2.3
Mean ± SD of fluoroscopy time, min
15.2 ± 9.7
16.0 ± 7.9
Median of serum urea, mg/dL
12 (5–24)
11.5 (7–17)
Mean ± SD of serum urea/serum creatinine
26.0 ± 6.9
29.1 ± 9.1
: Mann-Whitney U test, b: chi-square test; P < 0.05.
CIN: contrast-induced nephropathy; SD: standard deviation.
Table 3. Multivariate risk factors analysis for the development of contrast
induced nephropathy.
Risk factors
Odds ratio
[95% confidence interval]
0.1 [0.05–0.7]
0.2 [0.05–0.9]
Contrast media volume, mL/kg
0.3 [0.1–0.9]
Fluoroscopy time, min
0.1 [0.03–0.8]
Serum urea/serum creatinine
–0.2 [0.05–0.8]
Table 4. Main diagnoses of the patients.
Main diagnoses
No CIN (n = 30)
CIN (n = 16)
Ventricular septal defect
Patent ductus arteriosus
Aortic valve stenosis
Atrial septal defect
Tetralogy of Fallot
Coarctation of aorta
Transposition of great arteries
Dilated cardiomyopathy
Double outlet of right ventricle
Primary pulmonary hypertension
Corrected transposition of great arteries
CIN: contrast-induced nephropathy.
ÖZDEMİR et al. / Turk J Med Sci
Table 5. Comparisons of laboratory findings in the patients without and with contrast induced
Indicators of nephrotoxicity
No CIN (n = 30)
CIN (n = 16)
Before angiography
0.43 (0.32–0.79)
0.38 (0.31–0.67)
After 4 h
0.48 (0.34–0.79)
0.49 (0.31–0.73)
After 24 h
0.48 (0.35–0.83)
0.47 (0.34–0.83)
After 48 h
0.47 (0.35–0.77)
0.46 (0.36–0.94)c
Before angiography
0.54 (0.3–1.11)
0.58 (0.3–0.80)
After 4 h
0.61 (0.3–0.91)
0.64 (0.5–0.97)c
After 24 h
0.58 (0.3–1.02)
0.62 (0.4–0.90)c
After 48 h
0.62 (0.33–1.03)
0.65 (0.3–0.90)c
Before angiography
26.4 (1.9–226)
23.2 (5.3–40.8)
After 4 h
26.6 (4.4–214)
28.9 (3.6–153)
After 24 h
24.4 (1.7–195)
24.0 (5.8–48.6)
Serum creatinine (mg/dL)
Serum cystatin C (mg/L)
Serum NGAL (ng/mL)
After 48 h
27.6 (4.7–91.2)
22.5 (2.3–41.1)
Before angiography
4.1 (0.6–67.1)
5.1 (0.6–64.1)
After 4–8 h
2.2 (0.6–27.4)
2.3 (0.6–104)
After 48 h
2.8 (0.6–74.5)
6.3 (0.5–56.6)
Before angiography
5.6 (1.2–476)
13.9 (1.3–62.6)
After 4–8 h
8.2 (0.8–850)
20 (1.5–271)
After 48 h
5.5 (0.8–123)
18.9 (1.3–420)
Urine NGAL (ng/mL)
Urine NGAL/urine creatinine (ng/mg)
: Comparisons of the patients without and with CIN, Mann–Whitney U test; P < 0.05.
: Comparisons between hours in the patients without or with CIN, Friedman repeated measures
ANOVA; P < 0.05.
: Statistically significant difference between values prior to the angiography, Bonferroni corrected
Wilcoxon sign test; P < 0.05/4 = 0.0125.
CIN: contrast-induced nephropathy; NGAL: neutrophil gelatinase-associated lipocalin.
media use in all acute renal failure cases, as well (3,6,12).
Furthermore, CIN is known to have ranked third in causes
of mortality in postrenal failure acquired in hospitals
(5). However, today pediatric angiography patients can
be discharged within 24–48 h, with no CIN-induced
mortality or morbidity being expected or reported (12).
In the studies reporting postprocedural serum
creatinine follow-ups in pediatric angiography patients,
the patient groups were monitored for from 48 h to 2
weeks (9,12,17–20). Hirch et al. regarded a 50% or greater
increase in basal serum creatinine levels as significant
and found that 12% their patients developed CIN (9).
Sagy et al. showed that, in the pediatric patients with
cardiac angiography, left ventricular volume overload
was observed, and that, in those suffering from right-toleft shunt congenital heart disease with clinical left-sided
ÖZDEMİR et al. / Turk J Med Sci
heart failure, serum creatinine and uric acid levels rose to
a considerable extent (17). However, in other studies (18–
21), no change was observed in the serum creatinine levels
after having implemented the procedure. In our study, it
has been shown that risk factors are not effective in terms
of CIN development. However, in the patients diagnosed
with CIN, it has been observed that creatinine levels
substantially increased 4 h after the cardiac angiography,
and this increase was determined to be still in progress at
48 h, as well. This finding supports the idea that creatinine,
independent of risk factors, is effective in diagnosing CIN.
Kavukçu et al. administered iopromide, in a maximum
dose of 5 mL/kg with low osmolarity contrast media, to 19
children with congenital heart disease. In these patients,
no significant difference was observed in the levels of
serum creatinine, creatinine clearance, plasma uric acid,
plasma osmolarity, urine osmolarity, fractional excretion
of sodium, and urine N-acetyl-β-(D)-glucosaminidase
prior to and 48 h after angiography (20). As reported by
Noyan et al., in 17 cyanotic and 18 acyanotic children
with congenital heart disease, nonionic low osmolarity
iopamidol administration did not lead to CIN development
(19). In the subjects under 1 year of age and in those
administered more than 5 mL/kg of contrast medium,
the levels of urine N-acetyl-β-(D)-glucosaminidase,
β2‑microglobulin, and α1‑microglobulin were found to
be remarkably high 12 h after the procedure, and these
values were determined to have returned to normal in the
next 2 weeks, as well, by Niboshi et al. (18). In our study,
however, when comparing the subjects with and without
CIN, the baseline levels of nephrotoxicity biomarkers
were seen to have fallen short in anticipating the CIN
risk. Furthermore, in the patients diagnosed with CIN, no
significant difference was observed in serum NGAL levels,
urine NGAL levels, and urine NGAL/urine creatinine ratio
when compared to the values prior to the procedure. On
the other hand, serum CysC levels increased substantially
4 h after cardiac angiography, and this increase was found
to still persist at 48 h. This finding has led us to assume
that in CIN diagnosis and follow-ups, serum CysC is more
effective than NGAL.
In adult patients, it has been proposed that diabetes,
preexisting renal insufficiency, decreased renal perfusion,
and high total dose of contrast medium could be some
of the risk factors for nephropathy in the use of contrast
media (4,5). However, the risk factors of renal toxicity in
children with cardiovascular disease by using nonionic
contrast media have not been fully investigated (18).
The volume of contrast media administered during the
procedure, as the main modifiable risk factor, is of primary
importance in the development of CIN (4). However,
growing complexity of pediatric cardiac angiography
inevitably causes an increased use of contrast medium per
procedure and consequently enhances the risk of CIN.
The correlation between the amount of contrast and the
risk of CIN was documented in previous studies (5,18).
Administration of nonionic low osmolarity contrast media
(iopamidol, iohexol, ioversol) in cardiac angiography of 98
pediatric patients was shown to have increased the CIN
risk if contrast media exceeding 5 mL/kg was administered
(18). In the present study, we found that the risk of CIN
increased 2.29-fold if the volume of contrast medium
exceeded 4.1 mL/kg in children with congenital heart
disease undergoing cardiac angiography. The sensitivity
and specificity of the value were detected as 69% and
70%, respectively. Therefore, transient renal dysfunction
was also associated with the dose of the contrast medium,
i.e. children receiving more than 4.1 mL/kg of contrast
medium showed higher levels of renal tubular functional
parameters after angiography in this study. Although the
tubular dysfunction was transient, the administration of
large amounts of contrast medium should be avoided.
There is an agreement that adequate volume
expansion prior to administration of contrast media is
a major strategy in the prevention of CIN, although no
randomized controlled trials directly comparing a strategy
of volume expansion with no volume expansion have
been carried out to date (4). Although the pathogenesis
of CIN is not clearly understood, several mechanisms
such as alterations in renal hemodynamics (ischemia due
to vasoconstriction), direct tubular toxicity, oxidative
stress, and tubular obstruction are considered to be the
primary factors (4). Dilution of contrast media within the
tubule lumen, reduced activation of the renin-angiotensin
system due to increased delivery of sodium to the distal
nephron, and minimizing of reductions in the renal
production of nitric oxide caused by contrast media can
contribute to the beneficial effect of volume expansion
(22). Randomized studies demonstrated the positive effect
of adequate hydration in reducing rates of CIN (23–25).
Consequently, authors suggested adequate intravenous
volume expansion with isotonic crystalloid solution for 3
to 12 h before the procedure, to be continued for 6 to 24
h to prevent development of CIN, in these patients (26).
Only hydration with isotonic saline solution is accepted in
general as the best way to prevent CIN in clinical practice.
Although adequate hydration was assure and the volumes
of contrast media and baseline creatinine levels were
normal in our patients, the incidence of CIN was found
to be 34.7% in our study. Therefore, we suggest that the
incidence of CIN may be higher in pediatric patients with
congenital heart disease than in patients with other risk
4.1. Study limitations
This was a single-center study of pediatric patients with
congenital heart diseases receiving contrast media during
ÖZDEMİR et al. / Turk J Med Sci
cardiac catheterization. Therefore, the results will need to
be validated in a larger population. Moreover, the present
study was a cohort with normal kidney function, and it
will be important to confirm these findings in documented
high-risk settings such as volume depletion, concomitant
nephrotoxic drug use, and preexisting kidney dysfunction.
4.2. Conclusions
In this study in which patients with cardiac angiography
were taken into account, the CIN development rate was
found to be 34.7%. Therefore, our findings show that
the incidence of CIN is high in pediatric patients with
congenital heart disease. However, these patients were
asymptomatic and the course of CIN was benign. The
results indicate that nonionic contrast media should also
be used at minimal dosages for renal function in children
with congenital heart disease, because we note that the
use of nonionic contrast media leads to CIN. Especially in
patients receiving more than 4.1 mL/kg of contrast media
in total, we should be wary of CIN. On top of all this, in
comparing the children who received cardiac angiography
with the healthy ones, serum CysC, serum NGAL, and
urine NGAL levels and urine NGAL/urine creatinine
ratios were found to have fallen short in anticipating the
CIN risk. No difference was found among the patients in
terms of CIN risk factors. However, in the pediatric patients
who received cardiac angiography and were diagnosed
with CIN afterwards, the levels of serum creatinine and
serum CysC levels were found to be higher than the ones
measured prior to the procedure. Hence, it would be
sufficient to follow the renal functions of the pediatric
patients with cardiac angiography by monitoring their
serum creatinine levels. However, more comprehensive
studies into larger groups with such patients will be
required for further research.
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Cystatin C as biomarker of contrast-induced